11.8 Colon Flashcards
Defective relaxation and peristalsis of rectum and distal sigmoid colon
Hirschsprung disease
Hirschsprung association
Down syndrome
Plexus b/t IC and OL muscle layers of the muscularis propia that regulates motility
Myenteric (Auerbach)
Plexus in the submucosa that regulates BF, secretions, and absorptions
Submucosal (Meissner)
What causes Hirschsprung?
Failure of neural crest derived ganglion cells to descend into myenteric and submucosal plexus
- Failure to pass meconium
- Empty rectal vault on digital rectal exam
- Massive dilatation of bowel proximal to obstruction w/ risk for rupture
Hirschsprung
Hirschsprung rectal suction biopsy reveals
lack of ganglion cells
Tx Hirschsprung
Resection of the involved bowel (ganglion cells present proximal to diseased segment)
Outpouchings of mucosa and submucosa through the muscularis propria in colon (false diverticulum)
Colonic diverticula
Risk factors for colonic diverticula are related to wall stress
- constipation
- straining
- low fiber diet
- age (more common in older adults)
Where are colonic diverticula most commonly located?
where the vasa recta traverses the muscularis propia (weak point in colonic wall) most commonly in the sigmoid colon
Complications of colonic diverticula (though usually asymptomatic)
- Rectal bleeding (hematochezia)
- Diverticulitis
- Fistula
Presents with appendicitis-like symptoms in the LLQ
Diverticulitis (due to obstructing fecal material)
Inflamed diverticulum ruptures and attaches to a local structure; e.g. may present with air or stool in urine
Colovesicular fistula
Acquired malformation of mucosal and submucosal capillary beds
angiodysplasia
where does angiodysplasia usually arise?
cecum and righ colon due to high wall tension
rupture of angiodysplasia presents as
hematochezia in an older adult
AD disorder resulting in thin-walled blood vessels, especially in the mouth and GI tract; rupture presents as bleeding
Hereditary hemorrhagic telangectasia
Ischemic damage to the colon
ischemic colitis
most common location for ischemic colitis
splenic flexure (watershed area of SMA)
most common cause of ischemic colitis
atherosclerosis of SMA
ischemic colitis presentation
postprandial pain and weight loss
ischemic colitis –> infarction –> [presents as]
pain and bloody diarrhea
relapsing abdominal pain with bloating, flatulence, and change in bowel habits (diarrhea or constipation) that improves with defecation; classically seen in middle-aged females
Irritable bowel syndrome (IBS)
IBS is related to [cause]
disturbed intestinal mobility; no identifiable pathologic cahnges
what may improve IBS symptoms?
increased dietary fiber
raised protrusions of colonic mucosa
polyps
two types of colon polyps
hyperpalstic and adenomatous
polyps due to hyperplasia of glands; classically shows a serrated appearance on LM; most common
hyperplastic polyp
polyps due to neoplastic proliferation of glands; less common
adenomatous
hyperplastic polyps usually arise in the
left colon
benign polyp with no malignant potential
hyperplastic
benign, premalignant polyp (may progress to adenocarcinoma via adenoma-carcinoma sequence)
adenomatous
adenoma-carcinoma sequence describes the progression from normal colonic mucosa to
adenomatous polyp to carcinoma
three mutations in the adenoma-carcinoma sequence
APC, K-ras, p53
mutation (sporadic or germ line) that increases risk for formation of polyp
APC
mutation that actually leads to formation of polyp and increases its size
K-ras
mutation that allows for progression of adenomatous polyp to carcinoma
p53, requires increased COX expression
how to impede adenoma-carcinoma sequence?
ASA
risk for adenomatous polyp –> carcinoma is related to
size (>2 cm),
sessile growth,
villous histology
AD disorder characterized by 100s to 1000s of adenomatous colonic polyps
FAP
FAP due to mutation in
APC (chromosome 5)
Prophylactic treatment in FAP
remove colon and rectum (o/w almost all pts develop carcinoma by 40)
FAP with fibromatosis and osteomas
Gardner
non-neoplastic proliferation fo fibroblasts; arises in retroperitoneum (desmoid) and locally destroys tissue
fibromatosis
benign tumor of bone that usually arises in skull
osteoma
FAP w/ CNS tumors (medulloblastoma and glial tumors)
Turcot syndrome
sporadic, hamartomatous (benign) poly that arises in kids < 5yo; usually presents as solitary rectal polyp that prolapses and bleeds
Juvenile polyp
characterized by multiple juvenile polyps in stomach and colon; large #s inc. risk of carcinoma
juvenile polyposis
Hamartomatous (benign) ploys throughout GI tract and mucocutaneous hyperpigmentation (freckle-like spots) on lips, oral mucosa, and genital skin; AD
Peutz-Jeghers Syndrome (AD)
Peutz-Jeghers increases risk for
colorectal, breast, and gynecologic cancer
most common pathway for colon cancer
adenoma0carcinoma sequence
second molecular pathway for colon cancer
microsatellite instability
repeating sequences of noncoding DNA; integrity of sequence (stability) is maintained during cell division
microsatellites
microsatellite instability indicates
defective DNA copy mechanisms (e.g. DNA mismatch repair)
HNPCC is due to inherited mutations in
DNA mismatch repair
HNPCC increases risk for
colorectal, ovarian and endometrial cancers
De novo colorectal carcinoma (not from adenomatous polyp) at young age; usually right-sided
HNPCC
screening for colorectal carcinoma
colonoscopy and fecal occult blood testing; begins at 50
Older adult with iron-deficiency anemia
colon cancer (right sided)
colon cancer that grows as napkin-ring lesion; presents with decreased stool caliber, LLQ pain, and blood-streaked stool
Left-sided
colon cancer that grows as a raised lesion; p/w iron-deficiency anemia (occult bleeding) and vague pain
Right-sided
Strep bovis endocarditis =
colon cancer
colon cancer most commonly metastasizes to the
liver
CEA is a serum tumor marker that is useful for
assessing treatment response and detecting recurrence, not for screening
most common location for left-seed colon cancer
rectosigmoid colon
